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Epithelial Mesenchymal Transition And Metabolic Reprogramming In Human Breast Cancer Cells
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Book Synopsis Epithelial-mesenchymal Transition and Metabolic Reprogramming in Human Breast Cancer Cells by : Yuvabharath Kondaveeti
Download or read book Epithelial-mesenchymal Transition and Metabolic Reprogramming in Human Breast Cancer Cells written by Yuvabharath Kondaveeti and published by . This book was released on 2015 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Epithelial-Mesenchymal Plasticity in Cancer Metastasis by : Mohit Kumar Jolly
Download or read book Epithelial-Mesenchymal Plasticity in Cancer Metastasis written by Mohit Kumar Jolly and published by MDPI. This book was released on 2020-12-29 with total page 512 pages. Available in PDF, EPUB and Kindle. Book excerpt: Recent studies have highlighted that epithelial-mesenchymal transition (EMT) is not only about cell migration and invasion, but it can also govern many other important elements such as immunosuppression, metabolic reprogramming, senescence-associated secretory phenotype (SASP), stem cell properties, therapy resistance, and tumor microenvironment interactions. With the on-going debate about the requirement of EMT for cancer metastasis, an emerging focus on intermediate states of EMT and its reverse process mesenchymal-epithelial transition (MET) offer new ideas for metastatic requirements and the dynamics of EMT/MET during the entire metastatic cascade. Therefore, we would like to initiate discussions on viewing EMT and its downstream signaling networks as a fulcrum of cellular plasticity, and a facilitator of the adaptive responses of cancer cells to distant organ microenvironments and various therapeutic assaults. We hereby invite scientists who have prominently contributed to this field, and whose valuable insights have led to the appreciation of epithelial-mesenchymal plasticity as a more comprehensive mediator of the adaptive response of cancer cells, with huge implications in metastasis, drug resistance, tumor relapse, and patient survival.
Book Synopsis Insights Into Metabolic Reprogramming by the Epithelial-mesenchymal Transition in Breast Cancer by : James Michael Arnold
Download or read book Insights Into Metabolic Reprogramming by the Epithelial-mesenchymal Transition in Breast Cancer written by James Michael Arnold and published by . This book was released on 2018 with total page 344 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis The Heterogeneity of Cancer Metabolism by : Anne Le
Download or read book The Heterogeneity of Cancer Metabolism written by Anne Le and published by Springer. This book was released on 2018-06-26 with total page 186 pages. Available in PDF, EPUB and Kindle. Book excerpt: Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
Book Synopsis Cell Stress, Metabolic Reprogramming, and Cancer by : Sergio Giannattasio
Download or read book Cell Stress, Metabolic Reprogramming, and Cancer written by Sergio Giannattasio and published by Frontiers Media SA. This book was released on 2018-08-31 with total page 68 pages. Available in PDF, EPUB and Kindle. Book excerpt: The present eBook presents one review, five mini-reviews, and an opinion article on the achievements and perspectives of studies on important aspects of cancer cell metabolic reprogramming whose mechanisms and regulation are still largely elusive. It also sheds light on certain novel functional components, which rewires cell metabolism in tumor transformation.
Book Synopsis Epigenetic and Metabolic Regulators of Breast Carcinogenesis by : Iman Mamdouh Talaat
Download or read book Epigenetic and Metabolic Regulators of Breast Carcinogenesis written by Iman Mamdouh Talaat and published by Frontiers Media SA. This book was released on 2024-07-23 with total page 168 pages. Available in PDF, EPUB and Kindle. Book excerpt: Breast cancer is the most common tumor in females worldwide. Cancer epigenetics and metabolic reprogramming are known cancer hallmarks. Recent advances in the field of epigenetics include histone modification, DNA methylation, and non-coding RNAs. In contrast to genetic modifications, epigenetics refers to a set of dynamic alterations. By controlling the on and off states of oncogenes and tumor suppressor genes, as well as re-engineering the tumor microenvironment, epigenetics plays a crucial role in the initiation and progression of carcinogenesis. Additionally, the complex process of metabolic reprogramming is required for both malignant transformation and tumor development, including invasion and metastasis. Furthermore, reprogrammed metabolic activities have been utilized to diagnose, monitor, and treat cancer patients. In tumor tissues, metabolic heterogeneity was found to take a role in the adaptation to the microenvironment drastic changes resulting from current therapeutic modalities.
Book Synopsis The Epithelial-to-Mesenchymal Transition (EMT) in Cancer by : Joëlle Roche
Download or read book The Epithelial-to-Mesenchymal Transition (EMT) in Cancer written by Joëlle Roche and published by MDPI. This book was released on 2018-04-09 with total page 261 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is a printed edition of the Special Issue "The Epithelial-to-Mesenchymal Transition (EMT) in Cancer" that was published in Cancers
Book Synopsis The Regulation of Lactate Metabolism in Epithelial-mesenchymal Transition of Human Breast Cancer Cells by : Denisse Tafur
Download or read book The Regulation of Lactate Metabolism in Epithelial-mesenchymal Transition of Human Breast Cancer Cells written by Denisse Tafur and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Lactate is both a metabolite of glycolysis, and a component of several signaling pathways. Although recent studies indicate that lactate is a critical regulator of cancer development, very little is known about lactate metabolism in the context of metastatic cancer. Epithelial-to mesenchymal transition (EMT) promotes metastasis by inducing invasive properties in epithelial tumors. To determine whether EMT induces metabolic alterations, we have studied two epithelial breast cancer cell lines and their respective EMT-induced mesenchymal progeny for changes in lactate metabolism. Metabolic analysis revealed that EMT induced an enhanced glycolytic profile in mesenchymal breast cancer cells. In contrast, epithelial breast cancer cells preferentially use oxidative phosphorylation (OXPHOS) to produce ATP. The strong expression of the lactate importer MCT1 in epithelial breast cancer cells may involve the ERα-inducible GATA3 transcription factor. We detected a specific GATA3 binding site in the DNAse-hypersensitive region within the promoter of MCT1 gene and found that knockdown of GATA3 represses MCT1 expression. We also observed that the endogenous lactate receptor, G-protein coupled receptor 81 (GPR81), was highly expressed in epithelial breast cancer cell lines and hormone-positive breast cancer tumors. GPR81 regulated MCT1 expression and lactate uptake in epithelial breast cancer cells and its expression was crucial for cell proliferation and survival under nutrient-limited conditions. This study provides an overview of specific metabolic changes induced by EMT in two independent and substantially different epithelial breast cancer cell lines. In addition, we propose GPR81 as a potential prognostic marker and therapeutic target in hormone positive epithelial breast cancer.
Book Synopsis Tumor Cell Metabolism by : Sybille Mazurek
Download or read book Tumor Cell Metabolism written by Sybille Mazurek and published by Springer. This book was released on 2015-01-19 with total page 373 pages. Available in PDF, EPUB and Kindle. Book excerpt: The four sections of this book cover cell and molecular biology of tumor metabolism, metabolites, tumor microenvironment, diagnostics and epigenetics. Written by international experts, it provides a thorough insight into and understanding of tumor cell metabolism and its role in tumor biology. The book is intended for scientists in cancer cell and molecular biology, scientists in drug and diagnostic development, as well as for clinicians and oncologists.
Book Synopsis Metabolic Reprogramming During Breast Cancer Progression by : Albert Mao Li
Download or read book Metabolic Reprogramming During Breast Cancer Progression written by Albert Mao Li and published by . This book was released on 2022 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Cancer cells exhibit altered nutrient requirements and utilization compared to normal cells. A comprehensive understanding of the causes and consequences of these altered metabolic features can help inform the development of novel therapeutics aimed at impairing cancer cell proliferation and promoting differentiation, in addition to enriching our understanding of how cancer comes to be. In this thesis, we utilized breast cancer as a model to study how altered cell metabolism relates to differences in proliferative capacity and cell lineage identity. Using a targeted metabolomics approach, we discovered a metabolic signature suggestive of elevated serine and one-carbon (1C) unit metabolism in the aggressive, tissue-tropic metastatic subpopulations of triple-negative breast cancer cells. In line with previous reports, we confirmed a role for the oncogene c-Myc in driving the enhanced proliferation of the metastatic subclones compared to parental cells. Functional validation using genetic and pharmacologic inhibition approaches uncovered an exquisite dependency of metastatic cells on this mitochondrial pathway for growth in vitro and in vivo. Analyses of human breast cancer patient data further identified a significant association between high expression of mitochondrial serine and 1C unit pathway genes with patient mortality. In follow-up work, we determined that low serine levels drives a metabolic signature associated with breast cancer cell aggressiveness characterized by the transcriptional induction of genes involved in de novo serine synthesis and mitochondrial serine and 1C unit metabolism. A global transcriptome analysis uncovered serine starvation-mediated repression of estrogen receptor (ER) signaling in ER+ breast cancer cells, effectively converting them to an ER-- like state. Metabolomics, isotope tracing, and chromatin immunoprecipitation assays revealed a defect in glucose-derived central carbon flux leading to a loss of histone acetylation and silencing of ER pathway genes. Acetate supplementation rescued histone hypoacetylation and ER pathway activity, demonstrating that serine starvation influences breast cancer cell state through a metabolic and epigenetic regulatory axis.
Book Synopsis Epithelial-Mesenchymal Plasticity in Cancer Metastasis by : Mohit Kumar Jolly
Download or read book Epithelial-Mesenchymal Plasticity in Cancer Metastasis written by Mohit Kumar Jolly and published by . This book was released on 2020 with total page 512 pages. Available in PDF, EPUB and Kindle. Book excerpt: Recent studies have highlighted that epithelial-mesenchymal transition (EMT) is not only about cell migration and invasion, but it can also govern many other important elements such as immunosuppression, metabolic reprogramming, senescence-associated secretory phenotype (SASP), stem cell properties, therapy resistance, and tumor microenvironment interactions. With the on-going debate about the requirement of EMT for cancer metastasis, an emerging focus on intermediate states of EMT and its reverse process mesenchymal-epithelial transition (MET) offer new ideas for metastatic requirements and the dynamics of EMT/MET during the entire metastatic cascade. Therefore, we would like to initiate discussions on viewing EMT and its downstream signaling networks as a fulcrum of cellular plasticity, and a facilitator of the adaptive responses of cancer cells to distant organ microenvironments and various therapeutic assaults. We hereby invite scientists who have prominently contributed to this field, and whose valuable insights have led to the appreciation of epithelial-mesenchymal plasticity as a more comprehensive mediator of the adaptive response of cancer cells, with huge implications in metastasis, drug resistance, tumor relapse, and patient survival.
Book Synopsis The Role of Metabolic Reprogramming in Breast Cancer Progression and Metastasis by : Fanny Dupuy
Download or read book The Role of Metabolic Reprogramming in Breast Cancer Progression and Metastasis written by Fanny Dupuy and published by . This book was released on 2015 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: " Breast cancer is the most commonly diagnosed cancer in woman and the emergence of metastasis is the most deadly aspect of the disease. Major bioenergetic and biosynthetic demands are associated with proliferation in order to sustain the exponential growth of a primary tumor and metabolic pathways must be reprogrammed to meet these demands. However, the metabolic challenges of cells during tumor initiation will differ from those that occur during tumor progression and dissemination. Despite progress in understanding the underlying mechanisms of how altered metabolism fuels the growth of primary tumors, the role that metabolic reprogramming plays in the metastatic process remains poorly characterized. This work focused on identifying the regulators of metabolic reprogramming and defining their roles in mediating breast cancer growth and metastasis. Using transgenic mouse models, we showed that loss of LKB1 cooperates with ErbB2 to promote breast cancer initiation and progression at early stages. Loss of LKB1 resulted in the activation of mTOR signaling, conferring a pro-growth metabolic advantage to the tumors. However, LKB1-deficient tumor cells displayed greater sensitivity to glucose limitation compared to their LKB1-proficient counterparts, suggesting a lack of metabolic flexibility that was rescued by rapamycin-mediated suppression of mTOR signaling.To investigate the metabolic reprogramming associated with breast cancer progression we compared the metabolic profiles of breast cancer cells that originated from a single primary tumor; however, which display different abilities to metastasize. Our results reveal an overall increase in metabolic activity (glycolysis and OXPHOS) that correlates with an increase in metastatic potential. However, we demonstrated that upon dissemination, metastatic breast cancer cells engage distinct metabolic programs depending on the site of metastasis. Using breast cancer explants isolated from bone, lung or liver metastases, we demonstrate a bifurcation in the way these cells utilize available carbon sources. Mitochondrial metabolism is elevated in bone- and lung-metastatic cells while liver-metastatic breast cancer cells preferentially engage glycolysis. We next determined the molecular mechanisms responsible for the glycolytic switch observed in the liver-metastatic breast cancer cells. The transcription factor HIF-1[alpha] is activated in liver-metastatic breast cancer cells under normoxic conditions and partially responsible for the observed metabolic reprogramming. Downstream of HIF-1[alpha], PDK1 (pyruvate dehydrogenase kinase 1) was identified as an important driver of metabolic adaptation to energetic stress and was required for efficient liver metastasis. Our work demonstrates that, while loss of metabolic regulators may be advantageous for cancer initiation and early progression, retaining these key checkpoints is critical for metabolic adaptation to stress and successful metastatic dissemination." --
Book Synopsis Metabolism in Cancer by : Thorsten Cramer
Download or read book Metabolism in Cancer written by Thorsten Cramer and published by Springer. This book was released on 2016-08-24 with total page 272 pages. Available in PDF, EPUB and Kindle. Book excerpt: This textbook presents concise chapters written by internationally respected experts on various important aspects of cancer-associated metabolism, offering a comprehensive overview of the central features of this exciting research field. The discovery that tumor cells display characteristic alterations of metabolic pathways has significantly changed our understanding of cancer: while the first description of tumor-specific changes in cellular energetics was published more than 90 years ago, the causal significance of this observation for the pathogenesis of cancer was only discovered in the post-genome era. The first 10 years of the twenty-first century were characterized by rapid advances in our grasp of the functional role of cancer-specific metabolism as well as the underlying molecular pathways. Various unanticipated interrelations between metabolic alterations and cancer-driving pathways were identified and currently await translation into diagnostic and therapeutic applications. Yet the speed, quantity, and complexity of these new discoveries make it difficult for researchers to keep up to date with the latest developments, an issue this book helps to remedy.
Book Synopsis Cancer as a Metabolic Disease by : Thomas Seyfried
Download or read book Cancer as a Metabolic Disease written by Thomas Seyfried and published by John Wiley & Sons. This book was released on 2012-05-18 with total page 482 pages. Available in PDF, EPUB and Kindle. Book excerpt: The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburg's well-known theory that all cancer is a disease of energy metabolism. However, Warburg did not link his theory to the "hallmarks of cancer" and thus his theory was discredited. This book aims to provide evidence, through case studies, that cancer is primarily a metabolic disease requring metabolic solutions for its management and prevention. Support for this position is derived from critical assessment of current cancer theories. Brain cancer case studies are presented as a proof of principle for metabolic solutions to disease management, but similarities are drawn to other types of cancer, including breast and colon, due to the same cellular mutations that they demonstrate.
Book Synopsis In Vivo Metabolic and Vascular Response to Hypoxia in Twist Knockdown Murine Breast Cancer by : Brandon Sturgill
Download or read book In Vivo Metabolic and Vascular Response to Hypoxia in Twist Knockdown Murine Breast Cancer written by Brandon Sturgill and published by . This book was released on 2019 with total page 64 pages. Available in PDF, EPUB and Kindle. Book excerpt: Twist transcription factor is often overexpressed in aggressive tumors. Although needed in early embryonic development for organogenesis, Twist is known to induce an epithelial to mesenchymal transition in cells. In cancer, epithelial to mesenchymal transitions can lead to increased motility and invasiveness. It has also been linked to metabolic reprogramming and increased metastatic risk. Furthermore, metabolic preferences can increase proliferation, enhance metastatic potential, and influence the site of metastasis. We hypothesize that Twist directly affects the metabolism of cancer cells. We expect to see in vivo what we have seen in vitro; Twist overexpression should promote a shift away from glycolysis in response to reperfusion. To study the effects of Twist on metabolism in vivo tumors were grown in the dorsal skinfold window chamber and stressed by exposure to hypoxia. Knowledge of metabolism without information on the oxygen availability is incomplete because cell metabolism naturally shifts between oxidative phosphorylation and glycolysis in response to variations in oxygen availability. Knowing if oxygen is readily available is particularly important when studying cancer metabolism because tumors may have poor vasculature organization due to angiogenesis not keeping up with tumor growth. To know if metabolic changes are due to intrinsic or extrinsic factors hyperspectral imaging was used to determine vascular oxygenation within the tumor. Multiphoton microscopy was used to quantify metabolism on the cellular level by measuring the optical redox ratio as well as the relative contribution ratio of free and bound NADH. We found the optical redox ratio, vascular oxygenation, and hemoglobin concentration were affected more by hypoxia in the cell line not expressing Twist. This would suggest that Twist does have a direct impact on metabolism within the cell. Because multiphoton imaging was not performed during hypoxia, whether Twist causes quicker metabolic changes or causes resistance to metabolic change remains to be determined.
Download or read book Anoikis written by Steven M. Frisch and published by Springer Nature. This book was released on 2021-07-27 with total page 202 pages. Available in PDF, EPUB and Kindle. Book excerpt: Anoikis is defined broadly as apoptosis that is inhibited by appropriate cell-matrix interactions. Normal and tumor cells vary widely in their sensitivity to anoikis, but, in general, metastatic tumor cells are inevitably anoikis-resistant. In particular, tumor cells that possess a cancer stem cell or mesenchymal phenotype, arising from the oncogenic Epithelial-Mesenchymal Transition (EMT), are transcriptionally re-programmed to resist anoikis. While the anoikis response occurs through the mitochondrial pathway typically found in other apoptotic responses (e.g., DNA damage, death receptors, oxidative stress), the regulation of anoikis by cell-matrix signalling is unique and only partially characterized. The uniqueness of anoikis is: a. regulation by integrins, non-integrin matrix receptors, and the signaling complexes associated with them; b. regulation by metabolic changes occurring in response to attachment/detachment; c. regulation by oncogenes and tumor suppressor genes d. regulation by tumor microenvironment; e. regulation by EMT.
Book Synopsis REDEFINING THE MOLECULAR BASIS OF EPITHELIAL MESENCHYMAL TRANSITION IN BREAST CANCER METASTASIS by : Yubo Zhai
Download or read book REDEFINING THE MOLECULAR BASIS OF EPITHELIAL MESENCHYMAL TRANSITION IN BREAST CANCER METASTASIS written by Yubo Zhai and published by . This book was released on 2013 with total page 43 pages. Available in PDF, EPUB and Kindle. Book excerpt: Metastasis is a multi-step process that begins with cancer cells migrating and invading away from the primary tumor site and extravasating into distant organs to establish a secondary tumor. The loss of epithelial expression markers by neoplastic breast cancer cells in the primary tumor is believed to play a pivotal role during breast cancer metastasis. This phenomenon is the hallmark of the epithelial mesenchymal transition (EMT) process. Gene expression microarrays were performed to investigate key functional elements on an in vitro metastasis model derived from human breast epithelial cells (MCF-10F) treated with 17-beta estradiol. Functional profiling of dysregulated genes revealed progressive changes in the integrin signaling pathway, and epithelial-mesenchymal transition. In tumorigenic cells, the levels of E-cadherin, desmoplakin and various keratins were low, whereas SLUG, integrin beta 1 and fibronectin were high. SLUG, a zinc finger transcription factor acting as a transcriptional repressor, was defined as a promising target which led us establishing a SLUG-centered hypothetical pathway from the profile of dysregulated genes.
